ReviewJournal of translational medicine2025
Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Pathway dysregulation and therapeutic resistance in glioblastoma: molecular mechanisms and emerging therapeutic targets.Future science OA · 2026Review
- Overexpression of EZH2 is associated with clinicopathological parameters and poor prognosis in gliomas.Oncology letters · 2026Article
- Integrating Molecular Pathology, Tumor Microenvironment, and Novel Therapies to Overcome Resistance in Glioblastoma.Journal of molecular neuroscience : MN · 2026Review
- Review
- Single-Cell Multiomic Profiling Uncovers Radiation Dosage-Sensitive, Cluster-Specific Regulatory Dynamics in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Intercellular adhesion molecule 1 links glioblastoma biology to a scalable prognostic model integrating clinical, imaging, and molecular features.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Glioma represents the most prevalent primary tumors of the central nervous system, originating from glial cells. Cancer stem cells have the ability to extensively proliferate, self-renew, and form colonies, which contribute to tumorigenesis. Studies have found a population of cells within glioblastoma exhibiting characteristics similar to those of cancer cells, termed glioma stem cells (GSCs). GSCs have two distinct phenotypes: mesenchymal subtype (MES) and proneural subtype (PN). Despite the vital role of these subtypes in glioma biology, there is a significant lack of comprehensive reviews focusing on the regulatory mechanisms underlying each phenotype.This review integrates emerging insights into the regulatory mechanisms underlying GSCs plasticity, with dedicated analysis of novel pathways governing PN and MES phenotypes and their dynamic transition. By examining these critical elements, we aim to contribute to the development of novel therapeutic strategies in the ongoing fight against gliomas.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.